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EZHS42

Millipore

Human Amyloid β42 ELISA Kit

measures and quantifies Amyloid β42 levels in 50 μL CSF, cell culture supernatent or plasma

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About This Item

UNSPSC Code:
12161503
eCl@ss:
32161000
NACRES:
NA.84

product name

High Sensitivity Human Amyloid β42 ELISA, This High Sensitivity Human Amyloid β42 ELISA is used to measure & quantify Amyloid β42 levels in Neuroscience research.

Quality Level

200

species reactivity

human

packaging

kit of 1 × 96 wells

parameter

50 μL sample volume (Overnight assay)

assay range

sensitivity: 8.0 pg/mL
(50 μl sample size)
standard curve range: 16-500 pg/mL

technique(s)

ELISA: suitable

input

sample type plasma (K2 EDTA)
sample type serum
sample type cerebrospinal fluid (CSF)

application(s)

research use

detection method

colorimetric (450nm/590nm)

shipped in

wet ice

storage temp.

2-8°C

Gene Information

human ... APP(351)

General description

Amyloid beta peptides have been implicated in the etiology of Alzheimer’s disease. Amyloid beta 40 is the most prominent peptide and Amyloid beta 42 is the neurotoxic form. The Amyloid beta 42/40-ratio (AB ratio) has been reported as a better indicator of the Alzheimer pathology. Millipore’s High Sensitivity Human Amyloid β42 ELISA kit is used for the measurement of Amyloid β42 in cerebrospinal fluid, cell culture supernatants, primary neurons and plasma in a 96-well format.

Specificity

The Amyloid β42 ELISA (HS) uses monoclonal anti-Aβ antibodies with high selectivity for human Aβ. The capture antibody recognizes the C-terminal end of Amyloid β1-42, which causes a high selectivity for Aβ42. The cross-reactivity of the used antibodies to other Amyloid peptides was tested by ELISA and BIACORE and shows no significant cross-reactivity to Aβ1-38, Aβ1-39, Aβ1-40, Aβ1-43 and Aβ1-44.

Application

Research Category
Neuroscience
Research Sub Category
Alzheimer′s Disease
This High Sensitivity Human Amyloid β42 ELISA is used to measure & quantify Amyloid β42 levels in Neuroscience research.
This assay requires 50 µl of sample and is an overnight assay.
Used to detect/quantify: Amyloid β42

Storage and Stability

Components in the kit can be stored up to 2 weeks at 2-8°C

Other Notes

Please contact Technical Service for linearity of dilution.

Disclaimer

For research use only. Not for use in diagnostic procedures.

pictograms

CorrosionExclamation mark
GHS05,GHS07

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Warning

Hazard Classifications

Aquatic Chronic 3 - Met. Corr. 1 - Skin Sens. 1

Storage Class

8A - Combustible corrosive hazardous materials

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Teresa Niccoli et al.
Current biology : CB, 26(17), 2291-2300 (2016-08-16)
Glucose hypometabolism is a prominent feature of the brains of patients with Alzheimer's disease (AD). Disease progression is associated with a reduction in glucose transporters in both neurons and endothelial cells of the blood-brain barrier. However, whether increasing glucose transport
Gunjan Manocha et al.
Current Alzheimer research, 15(12), 1123-1135 (2018-08-03)
Alzheimer's disease (AD) is associated with age-associated central nervous system degeneration and dementia. This decline in the function correlates with deposition of Aβ peptide containing plaques and associated reactive gliosis. The inflammatory phenotype of microglia, in particular, is often considered
Nataliya Golovyashkina et al.
Molecular neurodegeneration, 10, 60-60 (2015-11-07)
Dendritic simplification, a key feature of the neurodegenerative triad of Alzheimer's disease (AD) in addition to spine changes and neuron loss, occurs in a region-specific manner. However, it is unknown how changes in dendritic complexity are mediated and how they
Kendra L Puig et al.
Journal of Alzheimer's disease : JAD, 44(4), 1263-1278 (2014-11-20)
Alzheimer's disease (AD) is a neurodegenerative disorder histologically characterized by amyloid-β (Aβ) protein accumulation and activation of associated microglia. Although these features are well described in the central nervous system, the process and consequences of Aβ accumulation in the enteric
Loukia Katsouri et al.
Neurobiology of aging, 34(4), 1105-1115 (2012-10-16)
Noradrenergic deficits have been described in the hippocampus and the frontal cortex of Alzheimer's disease brains, which are secondary to locus coeruleus degeneration. Locus coeruleus is the brain stem nucleus responsible for synthesis of noradrenaline and from where all noradrenergic
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